The overall objectives are (a) to introduce the new concept of systolic myocardial stiffness and test the hypothesis that end systolic myocardial stiffness in independent of end systolic stress (b) test the validity of this concept and the end systolic P-V relationship in the pathologic state. (c) establish the mechanical and hemodynamic correlates during the stable and decompensated states of LV hypertrophy induced by volume and pressure overload in conscious dogs. Serial studies will be conducted in the volume-overload model (AV fistula or aortic regurgitation) and pressure-overload models (aortic banding and perinephritic hypertension). Heart failure will be induced by superimposing a volume overload on dogs with severe aortic stenosis and compensated LV hypertrophy. LV volume calculations will be based on both the ultrasonic dimension technique and cineventriculography. More reliable assessments of myocardial function are needed for optimum timing of valve replacement in patients with chronic LV volume overload or pressure overload. These studies will provide a sound basis for the development of new myocardial function parameters, and a better understanding of the mechanisms involved in LV hypertrophy.